Molecular Mechanisms Linking Air Pollution-Induced Oxidative Stress to Inflammation and Human Disease.
6 affiliations
- 1School of Basic & Applied Sciences, K. R. Mangalam University, Gurugram 122103, HR, India.
- 2Department of Zoology, University of Rajasthan, Jaipur 302004, RJ, India.
- 3School of Sciences, Woxsen University, Hyderabad 502345, TL, India.
- 4School of Pharmaceutical Sciences, CGC University, Mohali 140307, PB, India.
- 5Department of Medicinal Chemistry, University of Florida, Gainesville, FL 32610, USA.
- 6Department of Biotechnology and Chemical Engineering, Manipal University Jaipur, Jaipur 303007, RJ, India.
Abstract
Air pollution is a major public health problem worldwide, causing millions of premature deaths every year due to its association with diseases of the respiratory, cardiovascular, neurological, metabolic and carcinogenic systems. A major mechanism of pollutant-induced toxicity has been well identified as oxidative stress. The overproduction of reactive oxygen/nitrogen species causes direct damage to cellular redox homeostasis and activation of inflammatory signaling pathways. This review provides a broad overview of the molecular mechanisms linking ambient air pollutants, such as particulate matter, nitrogen oxides, ozone, sulphur dioxide and volatile organic compounds, with health effects mediated by oxidative stress. Mitochondrial dysfunction, endoplasmic reticulum stress, and epigenetic reprogramming were critically discussed with key signalling pathways such as nuclear factor erythroid 2-related factor 2, nuclear factor kappa B (NF-κB), mitogen-activated protein kinase, and NOD-like receptor protein 3 inflammasome. Tissue-specific effects on respiratory, cardiovascular and nervous systems are also discussed. Susceptible populations and critical exposure windows are identified. Emerging advances in biomarker discovery, and mechanistic in vitro and in vivo approaches, are also summarized as promising tools to improve exposure assessment and disease prediction. Finally, current therapeutic approaches targeting oxidative stress and inflammation, as well as preventive measures to reduce pollutant exposure, are discussed to support precision environmental health and evidence-based air quality management.
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BibTeX
@article{awasthi2026molecular,
title = {{Molecular Mechanisms Linking Air Pollution-Induced Oxidative Stress to Inflammation and Human Disease.}},
author = {Kumud Kant Awasthi and Garima Awasthi and Rajbala Verma and Mahipal Singh Sankhla and Pallavi Saxena and Manpreet Kaur and Ruchi Pathania and Harsh Pandey},
journal = {Journal of xenobiotics},
year = {2026},
month = sep,
doi = {10.3390/jox16060185},
url = {https://europepmc.org/article/MED/42931071},
note = {CC BY},
}
RIS
TY - JOUR
TI - Molecular Mechanisms Linking Air Pollution-Induced Oxidative Stress to Inflammation and Human Disease.
AU - Kumud Kant Awasthi
AU - Garima Awasthi
AU - Rajbala Verma
AU - Mahipal Singh Sankhla
AU - Pallavi Saxena
AU - Manpreet Kaur
AU - Ruchi Pathania
AU - Harsh Pandey
PY - 2026
DA - 2026/09/26
JO - Journal of xenobiotics
DO - 10.3390/jox16060185
UR - https://europepmc.org/article/MED/42931071
AB - Air pollution is a major public health problem worldwide, causing millions of premature deaths every year due to its association with diseases of the respiratory, cardiovascular, neurological, metabolic and carcinogenic systems. A major mechanism of pollutant-induced toxicity has been well identified as oxidative stress. The overproduction of reactive oxygen/nitrogen species causes direct damage to cellular redox homeostasis and activation of inflammatory signaling pathways. This review provides a broad overview of the molecular mechanisms linking ambient air pollutants, such as particulate matter, nitrogen oxides, ozone, sulphur dioxide and volatile organic compounds, with health effects mediated by oxidative stress. Mitochondrial dysfunction, endoplasmic reticulum stress, and epigenetic reprogramming were critically discussed with key signalling pathways such as nuclear factor erythroid 2-related factor 2, nuclear factor kappa B (NF-κB), mitogen-activated protein kinase, and NOD-like receptor protein 3 inflammasome. Tissue-specific effects on respiratory, cardiovascular and nervous systems are also discussed. Susceptible populations and critical exposure windows are identified. Emerging advances in biomarker discovery, and mechanistic in vitro and in vivo approaches, are also summarized as promising tools to improve exposure assessment and disease prediction. Finally, current therapeutic approaches targeting oxidative stress and inflammation, as well as preventive measures to reduce pollutant exposure, are discussed to support precision environmental health and evidence-based air quality management.
SN - 2039-4705
SN - 2039-4713
ER -